LncRNA LINC00909 promotes cell proliferation and metastasis in pediatric acute myeloid leukemia via miR-625-mediated modulation of Wnt/β-catenin signaling.

Long non-coding RNAs (lncRNAs) have been shown to involve in a variety of cancers. Our present study aimed to explore the exact roles of lncRNA LINC00909 (LINC00909) in the progression of pediatric acute myeloid leukemia (AML) and to study the potential molecular mechanism. In this study, the levels of LINC00909 were observed to be distinctly upregulated in AML patients and cell lines. Higher levels of LINC00909 were associated with FAB classification, cytogenetics and poorer prognosis. Functionally, knockdown of LINC00909 suppressed cell viabilities, migration and invasion, and promoted apoptosis of NB4 and HL-60 cells. Mechanistically, we demonstrated that LINC00909 functioned as a molecular sponge for miR-625. In addition, we observed that Wnt/β-catenin signaling pathway was suppressed by LINC00909 knockdown. Moreover, miR-625 levels were dramatically decreased in AML cells when Wnt/β-catenin signaling was activated. Overall, our findings identified a new AML-related lncRNA LINC00909 which may represent a novel biomarker and a potential therapeutic target of AML. • LncRNA LINC00909 was highly expressed in acute myeloid leukemia. • LncRNA LINC00909 promoted the metastasis of acute myeloid leukemia cells. • LncRNA LINC00909 sponged miR-625 to regulate Wnt/β-catenin signaling. [ABSTRACT FROM AUTHOR]